Relation of membrane vesicles to volume and Na+ transport in smooth muscle: effect of metabolic and transport inhibition on fresh tissues.

Abstract

We tested the hypothesis that membrane vesicles of smooth muscle function as organelles controlling cell volume through a mechanochemical mechanism not involving Na+-K+ dependent membrane ATPase. Pieces of rat myometrium were incubated under various conditions at 25 degrees C, and then were analyzed after various times for Na+, K+, ATP and water contents or were prepared and examined in the electron microscope. Metabolic inhibition with iodoacetate (IAA) + dinitrophenol (DNP) rapidly depleted ATP, then decreased membrane vesicle number and increased vesicle size. Thereafter K+ loss, Na+ gain and water gain occurred. Slower depletion of ATP by treatment of tissues with IAA or ethacrynic acid produced similar, but delayed effects. Treatment with DNP alone, DNP in glucose-free Krebs-Ringer or glucose-free solution bubbled with N2 partly depleted the tissues of ATP but did not markedly affect the membrane vesicles or tissue water content. Ouabain affected neither ATP contents of tissues nor the numberof membrane vesicles, but produced large intracellular vesicles. The membrane vesicles were suggested to be sites of a mechanochemical volume control system.